Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medically Complex Patient > Dental Mgmt: Diabetes > Flashcards

Dental Mgmt: Diabetes Flashcards

1
Q

Diabetes can result from a combo of defects in both:

A

insulin secretion and action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diabetes affects the metabolism of what type of nutrient(s)?

A

every type (carbs, fats, proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

NIDDM sf:

A

Non-insulin dependent diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the body use if it cant’ use glucose?

A

FA –> ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The use of FA for energy can lead to:

A

ketoacidosis, triglycerides –> FA’s –> fuel source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does insulin maintain glucose homeostasis:

A

promoting glucose uptake into cells and storage in liver as glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Insulin promotes the uptake of these:

A

glucose, FA’s and AA’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TF? Cells can not use glucose as an energy source in diabetes.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does Type 1 diabetes affect insulin levels?

A

AI destruction of pancreatic B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

% of ppl w Type 2:

A

90%-95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Typical age for the onset of Type 1 diabetes:

A

15yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pts w Type 1 are more prone to have:

A

Grave’s, Addison’s, Hashimoto’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

TF? Some pts w DM have no evidence of autoimmunity.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What’s impaired in Type 2?

A

insulin function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Typically age of onset for type 2 diabetes:

A

40+, lower every yr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TF? Only minor Beta cell destruction in Type 2.

A

F. none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Is ketoacidosis more common in Type 1 or 2?

A

1, rare in Type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Types of diabetes:

A

AI, Type 2, gestational, pancreatic tumor, steroid induced, MRDM (malnutrition related DM), viral?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TF? Gestational DM usually stays w a woman after birth.

A

F. USUALLY goes away.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

TF? Women are more predisposed to Type 2 DM later in life if they get gestational during pregnancy.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ppl in US w diabetes.

A

29 million (8million undiagnosed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

% of pop in US w DM:

A

9.3%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

% pop over 65yo w DM:

A

26%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

of ppl w pre-diabetes:

A

86million and growing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pre-diabetic range, mg/dl:

A

100 - 126

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Diabetic, mg/dl:

A

126+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Normal, mg/dl::

A

under 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Risk factors for Type 2:

A

age, obesity, genetics, insulin resistant muscle, fat, and liver cells, abnormal liver glucose production, elevated glucagon levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Diabetics are __ times more likely to develop CV disease.

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diabetics are __ times more likely to have necrosis of extremities:

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diabetics are __ times more likely to have renal failure:

A

17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Diabetics are __ times more likely to go blind:

A

25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

TF? Insulin resistance is related to high cerebral glucose.

A

F. low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

TF? Insulin resistance is related to an inc risk of Alzheimer’s dementia.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does high fructose corn syrup affect a persons body?

A

alters metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

2 episodes of hypoglycemia increases a persons risk of developing dementia how many times?

A

2X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Vascular complications in diabetes results from:

A

microangiopathy and atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where do vascular changes occur in the body?

A

throughout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where are vascular changes most damaging in the body?

A

kidney and retina, brittle vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Molecular level changes that lead to vascular complications:

A

accumulation of polyols, adv glycation end products, inc VEGF, lipid deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Oral manifestations of vascular complications:

A

xerostomia, infection, poor healing, inc caries, gingival and perio problems, candidiasis, burning mouth, soft/hard tissue changes, bony changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Main complaint of diabetics:

A

dry mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does the dry mouth result from?

A

systemic dehydration, altered salivary flow, meds, autonomic dysfunction, altered BM of glands, fatty deposits in parotid gland (seen in HIV pts too)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is the viscosity of saliva altered w fat deposition?

A

increased viscosity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is the parotid gland affected by fat deposition?

A

enlarges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Effects of xerostomia:

A

caries (not pit and fissure), altered taste, burning mouth, discomfort, inability to swallow if severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Diabetic neuropathy may lead to:

A

burning, tingling, numbness, pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How to red oral burning and taste disturbances:

A

good diabetic control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Taste sense most likely to be affected by DM:

A

sweet, disordered glucose receps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

TF? Burning mouth syndrome is not really a syndrome.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Types of burning mouth:

A

1’ or 2’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which is idiopathic, 1’ or 2’?

A

1’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Burning mouth can be secondary to:

A

xerostomia, candidiasis, anxiety, depression, GERD, endocrine disorders, hormonal imbalance, esp. menopause, diabetes, hypothyroidism, nutritional deficiencies, esp Vit B, ZInc, Folate, and iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Ppl more likely to have a raw, depapillated tongue:

A

post menopausal, take blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Soft tissue changes that an occur:

A

exaggerated gingival response to plaque, similar to pregnancy gingivitis, hyperplastic, erythematous gingiva, acute gingival abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

A hyperplastic growth could be due to:

A

DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

1st identifiable oral manifestation of DM:

A

dramatic, aggressive pdd at a young age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pts w DM are more prone to these as a result of periodontitis:

A

acute gingival abscess (tartar of food in pseudopocket)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does DM promote periodontitis?

A

exaggerated inflammatory response to microflora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Are gingival crevicular fluid levels of glucose inc or dec in pts w DM?

A

inc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Effect of high gingival crevicular fluid levels of glucose:

A

changes interactions bw cells and their ECM in periodontium, good env for bad bacteria, inc production of end stage products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

AGE sf:

A

Advanced Glycation End-products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are AGE:

A

damaged proteins that accumulate and cause tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

AGE bind to:

A

mac and monocyte receptors and inc secretion of interleukin-1 & TNF-alpha- tissue destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What does AGE formation results in?

A

collagen build up in capillary basement membranes, dec perfusion, tissue destruction, dec ability to repair, inc risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Immunological changes:

A

dec wound healing, inc risk of infection, infection more likely to have severe sequelae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How to treat infections w DM pts?

A

aggressively, includes periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What causes dec wound healing?

A

Red phagocytic activity, delayed chemotaxis, vascular changes, abnormal collagen production, genetics, 1’ relative have some defects in collagen production wo having DM (may be familial component)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Why is an inflammatory response dec in extremities of pts w DM?

A

brittle vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Immunological changes are related to

A

immune status, inc risk for candidiasis & other fungal infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Fungal infections can lead to:

A

xerostomia, inc salivary glucose levels, immune effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Fungal infections of the mouth:

A

candidiasis, angular cheilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

When is angular cheilitis more common?

A

winter, dec VD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

When to assume a fungal infection is systemic:

A

if you can’t see where infection stops in oral cavity, dangerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How to treat hyperplastic candidiasis

A

debride, medicate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What does it mean if infection stops at denture line?

A

denture is infected, not as dangerous as systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How to treat fungal infection that stops at denture line:

A

topically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Issue w Rxing topicals to treat fungal infection:

A

pt compliance, pt thinks that are healed when they are not and should continue taking but they don’t and get reinfected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Mucosal mycosis:

A

fungal infection, AIDS, poorly controlled DM, starts as sinus or nasal infection, can perforate to OC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Tx duration of oral candidiasis:

A

2wks for all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

2 tx for oral candidiasis that are dissolved in mouth:

A

topical clotrimazole (5X/d), nystatin suppositories (6-8X/d)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

2 txs for oral candidiasis that are treated w 100mg and 200mg/d respectively:

A

Systemic Fluconazole, systemic ketoconazole

83
Q

Rhinocerebral Mucomycosis

A

Fungal infection caused mainly by Rhizopus oryzae, high risk of infection in those with DKA, presents as fever, nasal pain, ulceration, and necrosis with black nasal discharge, can spread quickly to brain

84
Q

Tx for Rhinocerebral Mucomycosis:

A

surgical debridement of tissues & intravenous lipid formulation amphotericin B starting at 5mg/kg/d w some doctors inc dose to 10mg/kg/d, control predisposing factors contributing to infection: hyperglycemia, metabolic acidosis

85
Q

DKA sf:

A

diabetic ketoacidosis

86
Q

a group of fungi that cause Rhinocerebral Mucormycosis:

A

Mucorales, mainly Rhizopus oryzae

87
Q

Does Rhinocerebral Mucormycosis have a high or low mortality rate?

A

high

88
Q

Pts most susceptible to Rhinocerebral Mucormycosis:

A

DM, immunocompromised

89
Q

What property of the fungus puts those with diabetic ketoacidosis at higher risk?

A

an enzyme that allows them to grow in a hyperglycemic, acidic conditions

90
Q

How are patients infected w Rhinocerebral Mucormycosis?

A

Spores inhaled through nose or lungs

91
Q

Presentation of Rhinocerebral Mucomycosis:

A

fever, congestion, pain, ulceration, necrosis, bloody or black nasal discharge, facial or periorbital swelling, dec vision &/ or double vision.

92
Q

There MIGHT be an inc incidence of this in pts w DM:

A

atrophic and erosive forms of lichen planus

93
Q

Which has a more sig inc in atrophic and erosive forms of lichen planus, Type 1 or 2?

A

Type 1

94
Q

What predisposes pts w Dm to oral infections?

A

poor control of it

95
Q

What dental tx, if any, can we do for well-controlled diabetics who lack secondary manifestations such as renal disease and cardiovascular involvement?

A

all indicated dental tx

96
Q

ASA categorization of well controlled DM:

A

ASA 2

97
Q

how to treat pts w medically compromising conditions

A

compromised treatment plans, more aggressive treatment, more antibiotics, more education

98
Q

Ways to measure how well Dm is controlled:

A

blood glucose or tolerance, A1C

99
Q

What is refractory hypertension:?

A

can’t get BP down NO MATTER WHAT

100
Q

What is brittle DM?

A

no matter what, you can’t get under control, if person is low, then high, etc. more likely to have complications

101
Q

TF? There might be an inc traumatic ulcers or fibromas in pts w DM.

A

T

102
Q

What does a glucometer measure?

A

capillary blood glucose level

103
Q

Fasting glucose req no food to be eaten for:

A

8h

104
Q

Blood glucose measurements that use capillary blood levels:

A

Random and fasting plasma and blood glucose (4)

105
Q

PPG sf:

A

Postprandial glucose

106
Q

Normal fasting blood glucose:

A

100mg/dl or less

107
Q

What is the glucose tolerance test?

A

give glucose, serial blood draws over a few hours, plot glucose curve

108
Q

What does the oral glucose tolerance test reflect?

A

rate of absorption, tissue uptake and excretion of glucose

109
Q

Is the oral glucose tolerance test taken while fasting or not?

A

while fasting

110
Q

how to take oral glucose tolerance test:

A

while fasting, give 100gm glucose, venous blood drawn before & at 1, 2 and 3hrs

111
Q

What would the oral glucose tolerance test for a diabetic show?

A

inc fasting, inc peak, & delayed return in 2 & 3h samples

112
Q

How many hours does it take for a pt with DM to dec blood sugar?

A

4-6h

113
Q

Pt w DM will have the highest BG level how long after eating sugar?

A

just after 1h

114
Q

What does A1C measure?

A

glucose bound to Hb, control over past 2-3mo

115
Q

Life span of RBC:

A

120d

116
Q

TF? A1C can tell you how well controlled a pts blood glucose is that day.

A

F. over last 3mo

117
Q

Nomal A1C value:

A

4.5-5.8

118
Q

ADA recommends A1C level to be below:

A

7%

119
Q

Over __% is considered poor control for A1C levels:

A

8%

120
Q

Prediabetic A1C range:

A

5.90-6.4%

121
Q

A1C level for diabetic:

A

6.5% +

122
Q

Hemoglobin A1C of 6 = ___ eAG(mg/dl)

A

125

123
Q

Hemoglobin A1C of 8 = ___ eAG(mg/dl)

A

183

124
Q

Hemoglobin A1C of 10 = ___ eAG(mg/dl)

A

240

125
Q

Hemoglobin A1C of 12 = ___ eAG(mg/dl)

A

298

126
Q

eAG sf:

A

estimated average glucose

127
Q

A1C must be higher than this to dx DM:

A

6.4

128
Q

At what A1C level does risk of diabetic retinopathy increase?

A

6.5%

129
Q

What is the most sensitive indicator of a high A1C?

A

retinopathy, dilated eye exam at opthomolagist, sensitive to changes in blood glucose

130
Q

If a pt has neuropathy they probably have:

A

early renal involvement

131
Q

Order of which 2’ issues are likley to present in DM pts:

A

microalbuminuria, neuropathy, nephropathy, retinopathy

132
Q

What can happen to preanalytic samples?

A

can undergo glycolysis

133
Q

The same sample in a lab for 2d can vary this much:

A

14%

134
Q

Is the intraperson A1C test variability high or low?

A

high

135
Q

Pop w higher A1C values for given glycemia levels:

A

African Americans

136
Q

T?F? A1C tests can have differences bw groups.

A

T

137
Q

Criteria for Dm dx for the different tests:

A

A1C > 6.5%, FPG > 126mg/dl, 2h PG > 200 mg/dl during OGTT, RG >200mg/dl in pt w signs & symptoms of hyperglycemia

138
Q

OGGT sf:

A

Oral glucose tolerance test

139
Q

Prediabetes: IFG:

A

100-125 (fasting glucose), <140 (2h after eating or 75gm OGTT)

140
Q

Prediabetes: IGT:

A

< 100 (fasting glucose), 140-199 (2h after eating or 75gm OGTT)

141
Q

Diabetes: IGT:

A

> or = to 126 or > 200 2h after eating or 75gm OGTT, needs confirmatory test OGTT, fasting or metabolic decomp

142
Q

How much does a 1% drop in A1C reduce the chance of vision loss, kidney failure, and nerve damage?

A

35%

143
Q

What’s more important to us in clinic, A1C value or blood sugar at that moment?

A

blood sugar at that moment

144
Q

Is Dm curable?

A

no

145
Q

Goals for mgmt of DM:

A

normal glucose, normal w8, control hypertension/ hyperlipidemia, develop a plan that doesn’t dominate a patients life

146
Q

Meds for DM:

A

Sulfonylureas, Meglitinides, Biguanides, Glucosidase Inhibitors, thiazolidinediiones

147
Q

Med for DM that stimulate insulin secretion:

A

Sulfonylureas, Meglitinides

148
Q

DM med that decreases glycogenolysis and hepatic glucose production:

A

biguanides

149
Q

DM med that dec GI absorption of carbos:

A

glucosidades inhibitors

150
Q

DM med that enhances tissue sensitivity to insulin:

A

thiazolidinediiones

151
Q

Rapid acting insulin meds:

A

Novalog, Humalog (3-5h duration)

152
Q

Short acting insulin meds:

A

Novalin R, Humalin R (5-8h duration)

153
Q

Intermediate-acting NHP insulin meds:

A

Novalin N, Humalin N (12-16h duration)

154
Q

long-acting insulin meds:

A

Levemir, Lantis (20-26h duration)

155
Q

Pre-mixed combo insulin meds:

A

Humalin 50/50. Novalog 70/30 (10-16h duration)

156
Q

Drug of choice for Type 2 diabetes:

A

Metformin

157
Q

These are often used in conjunction w insulin:

A

oral meds

158
Q

TF? If a person takes meds they have Type 1 DM.

A

F

159
Q

Which type of DM is more likely to be taking meds?

A

Type 2 (doesn’t make sense to me)

160
Q

TF? They only give insulin pumps to pts that can’t control their BG levels well on their own.

A

F. only pts w good control

161
Q

New approaches to meds:

A

oral/ inhaled insulin, injectable hormone analogs, stem cell therapy to create more pancreatic islet cells, antibody therapy

162
Q

Post-op gastric bypass, intestines produce:

A

GLUT-1

163
Q

Is there an inc or dec in inflammation post-op gastric bypass suyrgery?

A

dec

164
Q

TF? Gastric bypass can have benefits before weight losss.

A

T

165
Q

% relapse after gastric bypass surgery:

A

30%

166
Q

Which uses more energy to absorb sugar in the body, intestinal or gastric absorption?

A

gastric (check) aI assume bs if you have gastric you have both

167
Q

TF? A pt can immediately become non-diabetic after gastric bypass surgery.

A

T. seems the stomach is not absorbing the carbs, hormonal influence on small intestines?

168
Q

What can a prediabetic person do to red risk of developing diabetes by 58%?

A

lose 5-7% of their weight, exercise 1/2h daily

169
Q

Complications of metabolic syndrome:

A

obesity, hypertension, diabetes, hyperlipidemia, low HDL

170
Q

This is a pro-inflammatory state:

A

metabolic syndrome, high CRP and other inflammatory mediators

171
Q

Cardinal symptoms of undiagnosed diabetes:

A

Polyuriea, Polydypsia, Thirsty, Hungry, Sudden unexplained weight losses/gain

172
Q

Risk level a a pt w undiagnosed DM:

A

high risk

173
Q

What to ask pt w DM:

A

well controlled? frequency of testing, normal morning reading, readings today & yesterday, take meds & eat today?

174
Q

Who do we take blood sugar for?

A

Pt w diabetes who did not test that day

175
Q

Stress increases:

A

epi, corticosteroids, glucose and free fatty acid

176
Q

Stress decreases:

A

insulin

177
Q

High levels of this will increase blood glucose:

A

cortisal

178
Q

Can stress levels affect how well a pt controls their DM?

A

yes

179
Q

Refractory spike in blood glucose is due to:

A

stress, stimulates glycogenolysis

180
Q

TF? Significantly increased RBG presents an immediate safety risk.

A

F, indicator of poor control, detrimental to overall health

181
Q

Dental care can be continued up to this RBG reading:

A

400 mg/dl

182
Q

If a pts RBG is in this range for a few appt they shoudl be refered to thier PCP:

A

high 300’s

183
Q

Healthy pt RBG range:

A

100-150

184
Q

TF? Pts wo diabetes can become symptomatic at higher lood sugar levels than pts w DM.

A

F. vice verssa

185
Q

Give a pt sugar if their RBG reading is:

A

below 80 mg/dl

186
Q

Normal fasting glucose:

A

68-100

187
Q

Who is symptomatic earlier w changes in blood glucose, diabetic or non-diabetic?

A

diabetic

188
Q

Am or Pm appts for diabetics?

A

am, take meds, eat

189
Q

If a diabetic pt is shaking are they hypo or hyperglycemic?

A

hypo

190
Q

If a pt is taking both injections and oral meds for their DM, do they have Type 1 or Type 2?

A

Type 2

191
Q

Do this post-op for diabetic pts:

A

antibiotics, treat infections aggressively to cure, regain control of DM

192
Q

Why do diabetics have an inc risk of post-op infection?

A

delayed wound healing

193
Q

“Non por oss” means?

A

nothing by mouth

194
Q

Sedation pts:

A

NPO, careful protocols, ie 1/3 usual insulin and intra-op IV glucose

195
Q

Why might diabetic pts not be able to be tipped back all the way in the dental chair?

A

GI problems due to meds (glucophage)

196
Q

Steroid use is related to hypo/ hyper glycemia.

A

hyper

197
Q

ASA is related to hypo/ hyper glycemia.

A

hypo

198
Q

Low blood sugar symptoms:

A

sweating, headache, shaking, tired, weak, hungry, personality change

199
Q

Reasons for hypoglycemia

A

New or overmedications, missed meals, low carb meals

Increased activity, weight loss, alcohol, early pregnancy, kidney failure, menstrual cycle, gastroparesis

200
Q

TF? If a pts blood sugar levels are high it is dangerous to give them more sugar.

A

F.won’t make a difference

201
Q

Best juice to give to person w low blood sugar:

A

apple, absorbs faster than orange

202
Q

Glycemic index of sugar sources:

A

glucose = 100, sucrose = 65, orange juice = 47, milk = 35

203
Q

Should diabetics have more frequent recalls?

A

yes

Medically Complex Patient (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions